The diverse anomalies observed in CMCS patients can be understood in the context of three cellular phenomena: (1) the production and stability of the predicted truncated proteins, (2) the loss of GoLoco domains that are required for interaction with Gαi, and (3) the loss or maintenance of domains that can impact on other binding partners of Gpsm2. The gene discussed is GPSM2; the disease is Chudley-McCullough syndrome.